Each of these models was crossed into a Tigarfl/fl strain to generate pancreatic tumors that retained Tigar expression (CTR) or deleted (KO) for Tigar. Initial analysis of preneoplastic PanIN in the KC model showed that loss of TIGAR delayed the appearance of each stage of PanIN progression (PanIN1, 2, and 3), accompanied by lower proliferation in the Tigar null lesions, measured by Ki67 staining (Figures 1A–1D). This evidence concerns the gene MKI67 and pancreatic neoplasm.